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Signal strength and signal duration define two distinct aspects of JNK-regulated axon stability

Authors
Journal
Developmental Biology
0012-1606
Publisher
Elsevier
Publication Date
Volume
339
Issue
1
Identifiers
DOI: 10.1016/j.ydbio.2009.12.016
Keywords
  • Jun N-Terminal Kinase
  • Fos
  • Jun
  • Ap-1
  • Axonal Morphogenesis
  • Neurodegeneration
  • Neural Development
  • Drosophila
Disciplines
  • Biology

Abstract

Abstract Signaling proteins often control multiple aspects of cell morphogenesis. Yet the mechanisms that govern their pleiotropic behavior are often unclear. Here we show activity levels and timing mechanisms determine distinct aspects of Jun N-terminal kinase (JNK) pathway dependent axonal morphogenesis in Drosophila mushroom body (MB) neurons. In the complete absence of Drosophila JNK (Basket), MB axons fail to stabilize, leading to their subsequent degeneration. However, with a partial loss of Basket (Bsk), or of one of the upstream JNK kinases, Hemipterous or Mkk4, these axons overextend. This suggests that Bsk activity prevents axons from destabilizing, resulting in degeneration and overextension beyond their terminal targets. These distinct phenotypes require different threshold activities involving the convergent action of two distinct JNK kinases. We show that sustained Bsk signals are essential throughout development and act additively but are dispensable at adulthood. We also suggest that graded Bsk inputs are translated into AP-1 transcriptional outputs consisting of Fos and Jun proteins.

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